ArticleOncotarget2017
Inhibition of lysophosphatidic acid receptor ameliorates Sjögren's syndrome in NOD mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Cluster Analysis of Dry Eye Disease Models Based on Immune Cell Parameters - New Insight Into Therapeutic Perspective.Frontiers in immunology · 2020Pooled it
- Lysophosphatidic Acid (LPA) Salivary Species Detection and Whole-mount LPA Receptor Localization in Mouse Salivary Gland.bioRxiv : the preprint server for biology · 2026Article
- Lipid Metabolism: An Emerging Player in Sjögren's Syndrome.Clinical reviews in allergy & immunology · 2025Review
- A Mechanistic Insight into the Pathogenic Role of Interleukin 17A in Systemic Autoimmune Diseases.Mediators of inflammation · 2022Review
- Research progress on inflammatory mechanism of primary Sjögren syndrome.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Review
- Lysophosphatidic Acid Receptors: Biochemical and Clinical Implications in Different Diseases.Journal of Cancer · 2020Review
- Small Interfering RNA Targeting α-Fodrin Suppressing the Immune Response of Sjögren's Syndrome Mice.Chinese medical journal · 2018Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lysophosphatidic acid (LPA), a bioactive lysophospholipid, is involved in the pathogenesis of chronic inflammatory and autoimmune diseases. In this study, we investigated the role of LPA/LPA receptor (LPAR) signaling in the pathogenesis of Sjögren's syndrome (SS). We found that autotaxin, an LPA producing enzyme, and LPAR1 and LPAR3 mRNA, and IL-17 mRNA were highly expressed in the exocrine glands of 20-week-old nonobese diabetic (NOD) mice, which show SS symptoms at this age, as compared with non-symptomatic 8-week-old NOD mice. In an adoptive transfer model using NOD lymphocytes, treatment with Ki16425, an LPAR1/3 antagonist, restored tear and saliva secretion and decreased symptoms of SS compared with the vehicle-treated group. IL-17 levels in serum and lacrimal glands were also significantly reduced by Ki16425 in recipient mice. In addition, Ki16425 treatment of 20-week-old NOD mice, which spontaneously developed SS, restored saliva volume. Treatment of NOD splenocytes with LPA induced the expression of IL-17 in a dose-dependent manner, and Ki16425 inhibited this increase. LPA stimulated the activation of ROCK2 and p38 MAPK; and inhibition of ROCK2 or p38 MAPK suppressed LPA-induced IL-17 expression. Our data suggest that LPAR signaling stimulates SS development by induction of IL-17 production via ROCK and p38 MAPK pathways. Thus, LPAR inhibition could be a possible therapeutic strategy for SS.
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